Hence, it could be inferred that exogenous H2S inhibited the proliferation, metastasis and invasion of HCC through inducing cell cycle arrest and apoptosis of HCC cells, and the suppression of the angiogenesis by suppressing the STAT3 pathway (Lu et al., 2014), which is consistent with the fact that the abnormal activation of STAT3 promotes tumor cell proliferation via increasing cyclin D1 level, and inhibits apoptosis via increasing the levels of Bcl-2, survivin, and Mcl-1 (Garcia et al., 2001). Here, CCND1 is linked to hepatocellular carcinoma.